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Bleeding & Clotting
A/Prof David Roxby SA Pathology Transfusion Service South Australia National Blood Symposium
“The Bleeding Truth”
Patient Blood Management
Aim to optimise, conserve and manage the patient’s own blood to minimise or avoid exposure to allogeneic blood
Changing from a product focus to a patient focus Patient specific team approach Results in improved patient outcomes
PBM = Good clinical medicine An approach to safe, quality patient care…BUT one size doesn’t fit all
It will be nice to only transfuse what is needed, based on level I data, finally balancing risk and benefit in data-driven fashion for the benefit of our patients.
J Holcomb Critical Care 2010;14:162
Optimise red cell
mass
Minimise blood loss & bleeding
Harness & optimise physio-logical
reserves
Anaemia Iron deficiency
Blood loss & bleeding
Transfusion
Planned, multi-modal team approach to blood conservation & transfusion, involving patient,
combination of strategies
Courtesy of A Thomson
Haemorrhage Bleeding is a major cause of in-hospital mortality following:
Cardiovascular surgery/procedures Organ transplantation Orthopaedic surgery Obstetrics Trauma
Haemorrhage: Causes 30-40% of trauma mortality Leading cause of death in first hour of arrival1 Responsible for more than 80% of OT deaths2
Accounts for nearly 50% of deaths in first 24 h2
Control commonly thwarted by coagulopathy [25-30%]3, 4
1. Acosta JA, et al. J Am Coll Surg. 1998;186:528-533; 2 2. Kauvar DS, et al. J Trauma. 2006;60:S3-S11 3. Schochl H, et al. Scan J Trauma, Resus & Emerg Med. 2012;20:15-25 4. Aubron C, et al. J Crit Care 2014;29:471.e11-471.e17
0%
100%
INSULT/DISEASE
GOOD THINGS Retrieval
?Scoop & Run ?Stay and Play
Triage Hypotensive resuscitation Trauma management teams Diagnosis Imaging Invasive
Damage control surgery versus definitively “fixing” the problem
Organ supportive therapy
BAD THINGS Pre-existing disorders Increasing Shock Trauma to vital organs Trauma Coagulopathy SIR MOF Sepsis Blood storage lesion Compounding medical disorders
(Myocardial, Respiratory, Renal
Time
Surv
ival
Resuscitation
Mortality
Courtesy of J Isbister
RED CELLS Fresh v LD v Aged
Are the stored red cell transfusions
restoring O2 delivery to the
tissues and O2 Consumption
Do the stored red cell transfusions
have a causal connection with the
development of MOF and Sepsis (ie
TRIM & Storage Lesions)?
What is the importance of Blood/Plasma
Viscosity?
What is the importance of Colloid
Oncotic Pressure?
CLEAR FLUIDS Crystalloid v Colloid
What is the best electrolyte
composition?
HAEMOSTASIS FFP, Cryo, Plts, rVIIa
What is the quality of stored platelet
concentrates?
When should FFP, Cryo and Platelets
be given?
What is the role of haemostatic
agents?
Local v Systemic
Courtesy of J Isbister
Clinical & Laboratory Issues
Identify haemostatic imbalance Before surgery
Is there a bleeding history or coagulopathy?
During surgery What is the cause of bleeding?
Plt function Excess fibrinolysis Factor deficiency Vs residual anticoagulant
What coagulopathy is developing?
After surgery If patient is bleeding, is it due to
Surgical problems? Excess heparin? Coagulopathy?
Surgery Post-op Recovery
Thrombosis
Clotting
Bleeding
Hemorrhage
Can We Predict Who Will Bleed?
Adapted from Lawson JH, et al. Semin Hematol. 2004;41(suppl 1):55-64.
• Who is likely to bleed or clot too much? • How do we optimize the patient’s physiology? • Which local haemostatic agents are effective? • Which systemic haemostatic agents are effective?
There Is a Difference Between Who Is at Risk and Who Will Bleed
Patients at Risk for Surgical Bleeding
Certain patients are at higher risk for surgical bleeding including: Patients taking:
Anticoagulant therapy - warfarin Anti-platelet therapy – clopidogrel
Patients undergoing Repeat surgical procedures Oncologic surgery Aortic surgery Cardiac surgery Neurologic procedures or neurosurgery Radical prostatectomy
Dialysis patients Trauma patients
Surgical or vascular component
Corrected by surgical intervention or embolisation
Coagulopathy component: more difficult to
control due to several interrelated mechanisms
Consumption of coagulation factors & platelets
Dilution of coagulation factors
Metabolic (eg, hypothermia, acidosis)
Inflammatory process due to tissue injury
Drugs (aspirin, clopidogrel, warfarin)
Haemorrhage
Tissue trauma is controlled
Initiation of transfusion is rapid
Normovolemia is maintained
Normothermia is maintained
Monitoring of haemostasis is ongoing
Coagulopathy is a late event
Haemorrhage/Transfusion in Elective Surgery
Transfusion in Elective Surgery
Pre-Op Assessment of Bleeding Risk Assessment of surgical risk Structured bleeding history - defining any bleeding diathesis Estimated quality & duration of haemostatic support required Consultation across specialties
Intra-Op Approach to Bleeding Key relationships & lines of communication Appreciation of significance of haemodilution Early Rx of coagulopathy Application of Haemostatic Resuscitation principles similar to massive
blood transfusion in trauma
Tissue trauma is massive & uncontrolled Initiation of transfusion may be late Hypovolemia & shock are present Temperature is not controlled => hypothermia Monitoring of haemostasis is late Coagulopathy occurs early
Trauma, Haemorrhage & Transfusion
Complications of Massive Transfusion Lethal Triad: Hypothermia, Acidosis, Coagulopathy
Adverse Outcomes
•Systemic inflammatory response syndrome
•Multi-organ failure
•Sepsis
•TRALI/ARDS
•Mortality
Secondary Haemorrhage
Controlled Uncontrolled Trauma Pregnancy
Primary Pregnancy Infection Malignancy Envenomation
TIMELINES Urgency Delays Shock
COMORBIDITIES Cardiorespiratory Liver, Renal, GIT
Acidosis
Hypothermia
Factor deficiencies ?Fibrinogen
Fibrinolysis
Coagulation inhibitors
Hypocalcaemia
Positive Replacement
& Negative
Storage lesions Colloids
CONTEXT & CAUSE TREATMENT
INTERVENTIONS
Courtesy of J Isbister
Definition: Failure of blood to clot normally in response to tissue injury from trauma, surgery or routine invasive procedures
Risk factors for coagulopathy
4 Major independent risk factors: Injury Severity Score: ISS > 25
pH: < 7.10
Systolic Blood Pressure < 70 mmHg
Hypothermia: < 34°C
All risk factors: 98% None of these risk factors - 1%
Cosgriff et al. J Trauma 1997; 42: 857–61
Coagulopathy
Acidosis Hypothermia
Deadly Triad
Challenges inherent to the management of bleeding
Represents a significant clinical challenge trauma, surgical, medical & obstetric scenarios
High mortality Poor planning Poor communication Infrequent or inappropriate laboratory monitoring Massive transfusion
Inappropriate use of blood products
Significant delay in ordering/administering plasma/fgn Failure to prevent hypothermia & low use of fluid warmers
Bleeding Management
Treating team
Blood products supplying
service
Lab services
Nurse
Communication
ED/ICU/Surgeon/ Anaesthetist/Physician
Haematologist Transfusion
Blood Service
• Pre-operative bleeding risk assessment
• Bleeding history • Drugs
• Anaemia management • Fe therapy • EPO
Strategies to Minimise Blood Requirements
•Maintain haemostasis
•Oxygen support
•Maintain normovolaemia
•Temperature
•Anti-fibrinolytics (TXA)
•Red cell salvage
•Drain salvage - re-infusion systems
•Goal directed therapy
•POCT
Alternatives in Bleeding Management
Blind therapy According to estimated blood loss 1:1:1 formula driven (RC:FFP:Plts)
Individualised therapy Routine lab results directed therapy [time delays] PoC directed therapy – algorithm based
Specific coagulation factor concentrates
Goals and End Points If physiologic derangements can be minimized with better
haemorrhage control and resuscitation early in care, likely that rates of later complications and mortality will decrease and outcomes improve Minimize delays in receiving products Correct products in appropriate volumes [ratios] and order to
maintain reasonable concentrations of all factors
Transfusion Guidelines - Clinical Aims
Maintain temp > 35˚C pH > 7.2 Base excess < -6 Ionised calcium > 1.1 mmol/L Hb >70 g/L Plt count > 50 x 109/L PT < 1.5 x normal INR < 1.5 aPTT < 1.5 x normal Fibrinogen > 1.0 g/L (APH/PPH >2.0g/L)
Avoid hypothermia, metabolic acidosis, electrolyte disturbance & haemodilution
Effect of Hypothermia
Effect on Platelets Temp 33-35°C results in reversible function defect Alteration in function of GP receptor proteins – vWF and plt GP1b/IX stop functioning
Effect on Coagulation Cascade Slows enzymatic reactions of the coagulation cascade
↓ activity by ~10% / 1°C fall Decreases hepatic synthesis of coagulation factors Increases fibrinolytic activity
Impairs thrombin generation CLOTTING STOPS! When occurs in conjunction with metabolic
acidosis, mortality can be as high as 90%
Hypothermia impairs thrombin generation and formation of platelet plugs and fibrin clots, and at the same time increases the clot lysis
resulting in coagulopathy and uncontrolled bleeding
Activity reduced at pH~7.1 for: FVIIa, VII/TF complex, Xa/Va complex
Global clotting factor enzyme activity decreased by 90% at
pH~7.1
Thrombin activity decreased by 70%
27
“Moving Toward Normal Haemostasis
Normal Haemostasis
Procoagulant
Activity
Anticoagulant Activity
Fibrinolytic Activity
Antifibrinolytic Activity
Bleeding
Clotting
Adapted from Lawson JH, et al. Semin Hematol. 2004;41(suppl):55-64.
28
“Moving Toward Normal Haemostasis
Topical Haemostatics Purified Factors, FFP, Cryo, PLTs
Aminocaproic acid Tranexamic acid
Heparin, Warfarin LMWH
t-PA, SK, UPA
Normal Haemostasis
Bleeding
Clotting
FFP=fresh frozen plasma; Cryo=cryoprecipitate; PLTs=platelets; SK=streptokinase; UPA=urinary-type plasminogen activator; LMWH=low-molecular-weight heparin.
Procoagulant
Activity
Anticoagulant Activity
Fibrinolytic Activity
Antifibrinolytic Activity
Adapted from Lawson JH, et al. Semin Hematol. 2004;41(suppl):55-64.
Therapeutic Goals
Judicious use of blood components to correct coagulopathy Treat early
Treat adequately
‘Too little, Too late’
‘Not too wet nor too dry’
Early goal-directed coagulation management Surgical bleeding ↔ coagulopathy
Goal Prevent/minimize coagulopathy Avoid unnecessary transfusions Minimize end organ dysfunction
Goals in Transfusion Therapy
Move from Unstable to Stable Restore circulating blood volume
Restore Oxygen carrying capacity of the blood (DO2) Fluid overload/underload Defective RC function Impaired Hb function ARDS
Avoid coagulopathy Restore/maintain haemostasis
Red Cells Donor RCs Scavenged RCs
Blood components Fresh Frozen Plasma (FFP) Platelets Cryoprecipitate [Fibrinogen] PCCs (FII, [FVII], FIX, FX) [rFVIIa]
Drugs Anti-fibrinolytic agents - Tranexamic acid
Bleeding Management
Red Cells
Why give these? Restore DO2
Maintain blood architecture / rheology Maintain contribution to haemostasis
Why not Immunomodulation Infection risk Independent predictor of mortality?
Haemostatic Resuscitation: RC Haemoglobin level ???≥80 g/L
O2 delivery (DO2) RCs promote marginalization of platelets - concentrate along
endothelium & remain almost seven times that of the average blood concentration
Hct correlates with BT In rabbits, BT ↑ when the Hct < 35% In humans, the BT ↑ 60% when HCT ↓ 15%
Hct to sustain haemostasis in the bleeding patient is unknown
Eberst & Berkowitz. Am J Med 1994
Red Cells
Last update: 2012 18 trials - 6264 pts No difference in adverse
events in restrictive regimes compared to liberal regimes.
Target (70-80 g/L)
The Ideal Haemostatic Agent
Will work within minutes Will clot inappropriate haemorrhage Will not clot working vessels Will not have side effects Will be easy to store and use Will be inexpensive
Coagulation factors
Prior to 1990 (approximately) Fresh, stored or modified whole blood Labile coagulation factors not a problem
Coagulation factors
•
• Since 1990 Use of packed red cells (30-60 mL of plasma) Coagulation factors have become an issue
Clotting Factors
Factor Molecular Weight Plasma Concentration (µg/ml)
Required for Hemostasis (% of normal concentration)
Fibrinogen 330,000 3000 30
Prothrombin 72,000 100 40
Factor V 300,000 10 10-15
Factor VII 50,000 0.5 5-10
Factor VIII 300,000 0.1 10-40
Factor IX 56,000 5 10-40
Factor X 56,000 10 10-15
Factor XI 160,000 5 20-30
Factor XIII 320,000 30 1-5
Factor XII 76,000 30 0
Prekallikrein 82,000 40 0
HMWK 108,000 100 0
What’s the Problem?
• Constant changes in treatment recommendations
• Variation in clinical practice
• Lack of good evidence to guide practice • Lack of randomised controlled trials
• Assumptions • Abnormalities of PT/INR correlate with risk of bleeding from procedure
• FFP use can correct abnormal PT/INR & reduce or eliminate risk of bleeding
• Inappropriate use of labile blood components • Exposing patients to risk with poor evidence for benefit
• Inappropriate use of FFP to normalise INR
Best Practice & Research Clinical Anaesthesiology 2013;27:141-160
Summary of Dilutional Coagulopathy
Blood Volume Lost & Coagulation Status in Massive Haemorrhage
Blood Volumes Lost
% BV Exchanged
% Residual Coag Factors
PT/aPTT (x normal) Fgn Plts
(x109/L)
One 70 30 <1.5 >1.0 >100
Two 85 15 >1.5 <1.0 50
Three ≥95 5 >1.8 <0.5 <50
Haemostatic Resuscitation: FFP
Remains controversial when and in what dose plasma should be transfused to massively bleeding patients
Optimal ratio of FFP:RCs remains to be established FFP:RC ratio >1:2 is associated with improved survival compared to
one <1:2 Goal directed management
Fresh Frozen Plasma (FFP)
Recommendations / Guidelines Patient Blood Management 2011
FFP:RBC > 1:2
“Evidence base is poor” “Survivor bias” No PoCT recommended
Is There an Optimal Ratio of FFP:RC?
Pro 1:1 – 1:2 Hirshberg et al. J Trauma
2003; 54:454-63. Math model
Maegele M et al. Vox Sang 2008. Retrospective
Gonzalez et al. J Trauma 2007;62:112-9. Retrospective
Duchenese J et al. J Trauma 2009;67:33-37. Retrospective
Teixeira P et al. J Trauma 2009;66:693-97. Retrospective
Mitra B et al. Injury 2010;41:35-39. Retrospective
Peiniger S et al. Crit Care 2011;22:15. Retrospective
Indifferent Rangarajan K et al. J Emerg
Trauma Shock 2011;4:58-63. Retrospective
Dirks J et al. Scand J Trauma 2010;18:65. Retrospective
Davenport R et al. J Trauma 2011;70:90-95. Prospective
Magnotti L et al. J Trauma 2011;70:97-102. Registry
Snyder C. J Trauma 2009;66:358-62. Retrospective – selection bias
Con 1:1 Scalea et al. Ann Surg
2008;248:578-84. Prospective Nienhaber U et al. Injury
2011;42:697-701. Matched pair analysis
Johnson J et al. Arch Surg 2010;145:973-977. Prospective
Edens JW et al. Trauma 2010;69:81-86. Prospective
Watson et al. J Trauma 2009;67:221-227. Prospective
Kashuk et al. J Trauma 2008;65:264-70. Prospective
Haemostatic Resuscitation: Plts
Platelets pivotal for haemostasis: low Plts increases mortality
The highest survival was established in patients who received both a high Plt:RC and a high FFP:RC ratio
Holcomb JB, et al. Ann Surg 2008, 248:447-458. Zink KA, Sambasivan CN, et al. Am J Surg 2009, 197:565-570.
Fibrinogen Primary Haemostasis – mediator for platelet aggregation
Ligand between activated platelets GP receptor IIb/IIIa has a high affinity of Fgn
Secondary Haemostasis Precursor for fibrin » clot strength
Most common clotting factor, usually first to fall to critically low levels Reduced Fgn associated with increased bleeding Reduced Fgn on arrival increases risk of death after trauma Hyperfibrinolysis key part of the acute traumatic coagulopathy Extremely low Fgn levels are seen in massive PPH Impaired polymerisation
Colloids Fibrin degradation products FXIII deficiency
Sequence of Critical Clotting Factor Concentrations
Coagulation Factors Critical Level Blood Loss
Fibrinogen <1g/l 142% (117-169)
Prothrombin 20% 201% (160-244)
Factor V 25% 229% (167-300)
Factor VII 20% 236% (198-277)
Platelets 50 x 109/L 230% (169-294)
• Most common clotting factor • Usually the first clotting factor to fall to critically low levels
Fibrinogen
PBM Fibrinogen < 1.0g/L – “indicative of critical derangement” “current guidelines recommend…keeping fibrinogen
above 1.0g/L”
“..insufficient evidence to identify… a fibrinogen level…to trigger a blood component transfusion”
Other guidelines (and authors) recommend fibrinogen > 1.5 or 2.0 g/L
Fgn, FVIII, vWF, FXIII, fibrinectin Stored frozen @<-20⁰C Dose: 2ml/kg body weight WB: 378 ± 125 mg/unit (vol: 37 ± 2 mL) (Std Dose: 10 bags) Apheresis: 856 ± 298 mg/unit (vol: 54-66 mL) (Std Dose: 5 bags)
Dose on mls/Kg not total gms Thawed cryoprecipitate self life 6 hrs Each unit ~ increases [Fgn] by 0.2 -0.4g/L Accurate dosing difficult Use when fibrinogen < 1.0 g/L despite FFP 1500mL of FFP = 300mL of cryoprecipitate = ~4g fgn
Cryoprecipitate
Fibrinogen and Clinical Benefit
August 2013 Six RCTs of elective surgery
Fibrinogen Concentrate reduces the risk of allogenic transfusion (RR 0.47)
No effect on other outcomes Trials: “Low quality,… high risk of bias,…
underpowered.”
Excluded 14 retrospective cohort studies
Peri-operative Coagulation Monitoring Rational diagnostic basis for pro- & anti-thrombotic interventions
in patients undergoing emergency & elective surgery Main goal of peri-operative monitoring of haemostasis is to:
increase safety of patients undergoing surgical procedures
50
Importance of Coagulation Monitoring
Diagnose potential causes of haemorrhage Predict risk of bleeding Guide appropriate haemostatic therapy
Blood products associated with increased LOS Infections & sepsis MOF Morbidity & mortality TRALI TACO
Standard coagulation assays
Often provide a specific biochemical diagnosis
No assurance that this correlates to the clinical picture
Adequate Haemostatic Function • Std coags or PoCT (ROTEM/TEG) • Correct blood products in
appropriate volumes • Anti-fibrinolytics
Identify Cause & Stop The Bleeding • Surgery • Physical measures • Embolisation • Minimise delay in
receiving products
Rational Haemostatic Function & End Points
How to Optimally Monitor & Assess Haemostatic Function
Require information on all aspects of haemostasis Knowledge of rate & amount of thrombin production PT & aPTT only report initial generation of thrombin based
on first appearance of clot Events that occur after initial thrombin generation are also
critical but ARE NOT assessed by PT & aPTT: Changes in fibrin assembly, structure and mechanical properties Platelet activation Fibrinolysis
Coagulation Pathway
The classic coagulation ‘cascade’ does not explain how blood clots in vivo
Coagulation There really are ‘Intrinsic’ & Extrinsic Pathways Not redundant – operate on different cell surfaces
‘Extrinsic’ or TF pathway works on the initiating cell ‘Intrinsic’ pathway works on platelet surface
Normal Haemostasis Is a Balance
Adapted from Lawson JH, et al. Semin Hematol. 2004;41(suppl 1):55-64.
•Trauma •Major Surgery • Haemophilia
• Stroke • MI • Thrombosis
Bleeding to Death
Clotting to Death
Blood coagulation Anticoagulation Fibrinolysis Anti-fibrinolysis Vascular tone and blood flow Endothelial cells and platelets
The Ideal ‘Global’ Assay?
Allow assessment of an individual’s haemostatic state Based on plasma or cell model of coagulation
Endpoint: clot formation or thrombin generation Incorporate platelet/membrane components Include fibrinolysis
Good correlation with clinical outcomes Thrombosis and bleeding risk Sensitive to various anticoagulants
Rapid, inexpensive Easy to use in routine lab or clinical setting
Which assay?
“All experimental systems, whether in vitro, ex vivo or in vivo are, in their own way, artificial, with limitations both known and unknown” Allen et al J Thromb Haem 2:402 2004
Standard Coagulation Tests
The commonly used clinical coagulation tests only reflect the adequacy of the coagulation factor levels in the pathway being tested
Each test only assays A PART of the components required
for haemostasis
Coagulation Monitoring 60 No appropriate tests available for use in complex surgery or
critical bleeding
Routine coagulation testing – limited for massive bleeding
Standard testing [PT/INR, aPTT, Fgn, Plts]: Not good predictors of transfusion requirements Indirect correlation with clinical picture Poor predictive value for bleeding
PT/INR – developed to monitor warfarin therapy
aPTT – developed to monitor heparin therapy
Fibrinogen (Clauss Method) may be over estimated by up to 30% in presence of infused colloids or starches
Standard Coagulation Tests
Stop measuring at first stage of coagulation, when the clot first forms
Platelet poor plasma tests - measures plasma haemostasis not patient haemostasis, which is in whole blood
Important role of RCs, plts and phospholipids in coagulation not taken into account
Plasma Clotting Analyses Shortcomings
Traditional plasma coagulation analyses return only information of clot formation start
Time [sec]
CoagulationFinal Clot
Clo
t for
mat
ion
Viscoelastic Coagulation Methods Growing evidence that rotational thromboelastometry (ROTEM) or
thromboelastography (TEG) are superior to conventional assays
Real-time measurement of visco-elastic properties of clot kinetics
Potential to guide coagulation therapy according to actual needs
Reduce risk of over or under transfusion – algorithm guided replacement
Cohort studies
Reduced transfusion requirements Reduced transfusion related adverse events Improved outcomes
Used in various clinical settings – liver transplant, cardiac surgery, obstetrics & trauma
High negative predictive value
normal results → bleeding highly unlikely due to significant coagulopathy
63
The Technology
Advantages Assesses broader picture of haemostasis Identifies mechanisms of massive intra-operative blood loss & trauma-
associated coagulopathy Clotting is induced under low sheer conditions (similar to rheologic
properties in venous system in vivo) Improved TAT for clinical therapy
Disadvantage Endothelial component not involved Activators result in generation of thrombin and may mask effect of anti-
platelet agents
Viscoelastometry
Functional assay Global assessment (from
initiation of coagulation through clot lysis)
Multiple end-points Reflect ability to monitor
thrombin burst Functional fibrinogen
Function How much used in clot
Factor Deficiencies Platelet Function Clot Strength Fibrinolysis
Thromboelastometry /Thromboelastography – Point of Care Use in the Acutely Bleeding Patient
- 66 -
The Role of Thrombelastography in Multiple Trauma Victor Jeger, Heinz Zimmermann, Aristomenis K. Exadaktylos Hemorrhage and traumatic coagulopathy are major causes of early death in multiply injured patients. Thrombelastography (TEG) seems to be a fast and accurate coagulation test in trauma care…to detect an acute traumatic coagulopathy and especially primary fibrinolysis….
“No beneficial effect on patient’s survival [no RCTs]”
BUT “Positive results on reducing bleeding and proportion of patients requiring transfusion (platelets and plasma)” 2011
POC Improves Outcome
Weber CF, Görlinger K, Meininger D et al. Point of care testing: A prospective randomized clinical trial in coagulopathic cardiac surgery patients.
Anesth 2012; 117: 531-47
152 – randomized to 100 Pts with complex surgery and adverse bleeding randomized to POC (RoTEM plus Multiplate) Vs conventional therapy
Primary Outcome: RC Usage 4.9 u (conventional) Vs 2.6 POC p<0.001
Secondary outcomes all less in POC: FFP, Plt ,Mech Vent time, LOS, 6 month mortality
Use of PoCT
Time efficient Clinically efficacious Cost effective Pathophysiology driven therapy Guiding selective blood component/anti-fibrinolytic use Reduce inappropriate transfusions Decreases variability in treatment
Surgical control (compression, pelvic compression, packing)
Basic conditions T>34°C, pH 7.2, Ca++>1mmol/L, Hb>80g/L
Aspirin, oral anticoagulants, heparin
Anti-fibrinolytics
Fibrinogen or Cryo
PCC or FFP
Platelets
rFVIIa FXIII
Therapeutic Considerations
Timing & Sequence of Interventions Correct pH & temp Explore traumatic/surgical source of
bleeding Avoid excessive dilution with
colloids/crystalloids First line substitution with Fgn Facilitate thrombin
generation with PCC or FFP Plt transfusion
Summary
Establish a multi-disciplinary approach Consider blood conservation strategies Blood transfusions are not benign - must be used in an
individualised goal directed manner in all patients Coagulopathy is an intricate multi-cellular & multi-factorial
process
PT & aPTT used as surrogate markers
Problems with conventional assays
Time lapse for reporting result
Insufficient identification of the haemostatic defect
Conclusion
Change in philosophy required From sending std coags or PoCT only when there is obvious bleeding Towards concept of routinely monitoring high risk patients throughout
resuscitation/surgery
PoCT results in: Fewer transfusions Improved outcomes
Informs clinical practice Identifies patients at risk Allows early identification & treatment of evolving coagulopathy No longer acceptable to manage bleeding patients on the basis of clinical
judgement & probabilities – invariably leads to increased transfusions
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